Renal mass increases in compensation for the ablation of nephrons and in response to a variety of stimuli. We propose to continue our investigation into the causes and mechanism of the compensatory growth. we will test the hypotheses that renal compensartory growth is regulated by humoral factors and that the cell membrane plays a critical role in its initiation and turn-off. We will specificatlly aim to determine: 1. The role of transferrin and iron as renal growth factors. 2. The role of irons in the initiation and turn-off of renal growth. 3. The role of the purine nucleotide cycle in compensatory adaptation. 4. Changes in the membrane at the onset of compensatoary adaptation, compared to changes of membrane regeneration after renal injury. We will focus on a comparison of growth after ablation of nephrons and the growth that accompanies acidosis. STudies of renal comnpensatory adaptation in the two models will enable us to investigate the factors that control cellular growth. Our long-term goal is to understand the control and augmentation of renal cellular growth and regenaration. We hope our findings can be applied to the achievement of optimal renal funmction in patients with destruction of renal tissue.